The present invention relates to a therapuetic apparatus, and more particularly to a device for stimulating intramuscular fluid pressure in order to provide relief of pain or other discomfort. Certain types of pain and other bodily discomfort do not respond well to medication. Alternative methods of treatment such as acupuncture and acupressure have their proponents. The art of acupressure is similar to the art of acupuncture, except that no needles are used in administering the treatment. Specifically, acupressure is the application of pressure to various body areas to affect nerve junctures within the body. The nerve junctures affected in order to provide temporary relief of pain or other bodily discomfort are often associated with the sciatic nerve, which is sensory and motor nerve originating in the sacral plexus and running through the pelvis and upper leg.
Many different devices have been advanced as optimal acupressure tools. Examples of such devices are the bodo, a device with the handle having thereon a single knob-like probe with an operating surface of approximately less than 1 square inch. This device is used by therapists and self-massage shiatsu technique to access small places typically inaccessible to the entire palm of the hand, the elbow, or other parts of the anatomy which traditionally have been utilized to accomplish massage. Another device is the apparatus disclosed in U.S. Pat. No. 4,520,798 to Lewis for a self accupressure method. Still another is the massage means disclosed in the U.S. Pat. No. 4,493,315 to Iwahashi. This particular massage means discloses a hand-held device having an intermediate stick having one end joined to the right hand bar and the other end joined to one end of the left hand bar, the center portion of the intermediate bar being made of resilient material and a pair of spherical pressing members disposed at both ends with respect to the center portion of the intermediate bar with a space provided therebetween in the longitudinal direction of the intermediate bar.
Chronic muscle pain has been shown to be related to specific regions of the body known as "trigger points" or "trigger zones". Although these terms were used as early as 1936 in the American Journal of Medical Science, it was not until 1938 that an article in the Journal of the American Association associated the pain phenomena with musculature.
Pathogenic muscular tension has negative affect on blood circulation and fluid pressure within the body. For example, muscle tension squeezes the blood vessels, clamping them closed and consequently inhibiting desired blood flow. With respect to the arteries, this tension reduces the flow of oxygenated blood through the tissues, a condition known as ischemia. This tension also results in the burning of food stuffs in the absence of adequate oxygen, a condition known as anaerobic metabolism. This in turn results in the production of lower amounts of energy due to incomplete combustion of glucose and the formation of lactic acid which affects the chemical balance in muscle tissue. The increased presence of lactic acid and its byproducts most importantly increase the acidity by decreasing the pH within the muscle tissues, a condition known as acidosis. The presence of increased levels of lactic acid stimulate the nociceptor or pain nerves resulting in a deep pain which spreads throughout the muscle tissue.
The tension affects on arteries also present increased resistance to blood flow thereby directly and indirectly contributing to an increase in blood pressure. Similarly, tension affects the blood flow through veins, since the thin and pliable vessels of venous circulation are extremely susceptible to occlusive pressures. The tension also increases resistance to flow of wastes such as lactic acids. Additionally, back pressure due to resistance to flow prevents fluids from leaving muscles, thereby resulting in myositis, increased fluid content in muscle tissue spaces.
As the muscles continue to fill with incompressible fluids, the internal muscle fluid pressure known as the hydrostatic pressure, rises. This fluid pressure results in afferent signals to the central nervous system that the muscle is experiencing an internal stretch, which is reponded to by motor neurons in the anterior horn that transmit signals to increase the contractions of the tensing muscle to counter the perceived stretching of the muscle fibers, a condition known as a stretch-reflex or myotatic reflex. This resultant involuntary muscle contraction continues and results in further increased muscle tension. The fluids which are in the muscles become locked into the tissue as the muscle further contracts. Muscle contraction forces fluids into paths of least resistance, especially into fascial and tendinous tissue. This condition is known as myofascitis. Fluid becomes sequestered in these relatively fibrous tissues that have little metabolic activity and diminshed channels available for circulation.
The pockets of fluid encourage focal myospasm and are associated with trigger points. Such trigger points are unrelieved by conventional therapy devices since such devices do not adequately relieve the fluid pressure in intramusclar tissue spaces.
The points from which pain is sensed is unclear, but these fluid sequestrations are palpable. Applying deep digital pressure to these "trigger points" may have relieving or aggravating effects upon the strength duration and/or character of pain perceived. It is the published opinion of lending medical researchers of myofascial trigger points that there are only three therapies that will defuse the trigger point: (1) spray with a vapocoolent spray and stretch the muscle, (2) inject the fluid/spasm nidus with a solution containing procaine, and (3) external pressure applied to the muscle (ischemic compression). See for example the article authored by Dr. Janet Travell entitled "Myofascial Origins Of Low Back Pain", Post Graduate Medicine, Feb. 1983.
Myofascial tension, or tension within the muscles and their coatings are known to pinch off channels of circulation, either by direct pressure or stretch. Lactic acidosis and a large group of other autotoxins result in nerves becoming more excited. The acidic and toxic irritation of muscle spindle afferents bombard the central nervous system with proprioceptive input and fire hyperirritable alpha type A motor efferents thereby increasing muscle contraction. Acidic, toxic and pathoreflexive irritation of gamma efferents increases the tension of muscle spindle intrafusal fibers, thereby increasing spindle sensitivity.
In addition to stagnating fluids presenting problems with focal sequestration, tension and acidosis, it also presents problems with intramuscular edema. The hydrostatic pressures associated with intramuscular edema, while relatively soft, help to perptuate a vicious cycle. Increased stiffness is a likely result of hypersensitive myotactic responses to congestive intramuscular edema. This stiffness is noted to occur following periods of rest where passive cyclic filling (congestion) and muscle tension summate as concommittants.
Prior to the 20th century, massage was the corner stone of pain therpy. However, beginning in the early 20th century medical professionals increasingly relied on the injection of analgesic at the location of the painful spot in the muscle.
Diffuse myofascial pain syndrome is defined by the International Association for the Study of Pain as a syndrome characterized by diffuse aching musculoskeletal pain and stiffness. Studies have attempted to define the basis for myofascial pain, with many of these studies focusing on the relationship between pain and trigger points or trigger zones. Unfortunately, as recently as 1989 Fishbain et al in article in the June issue of the Archives of Physical Medicine and Rehabilitation conceded that the etiology of diffuse/specific myofascial pain syndrome is unknown.
Prior acupressure devices have relied on the concept of addressing myofascial trigger point syndromes, as if specific trigger points are the source of all pain within the musculoskeleture. Consequently, they focused on point specific devices such as those which would have direct application to the Shiatzu mode of therapy.
Trigger point therapy art devices are specifically designed for "point by point" application to relieve fibrous adhesions, focal sequestrations of fluid and/or spasmodic neurological dysfunction. Thus, prior art therapy devices have consistently employed knob-like spherical or pointed contact surfaces. Such embodiments of prior art trigger point therapy devices do not address stimulation of intramuscular fluid reabsorption pressures, or "decongestive compression" therapy.
According to Starling's Law of capillary dynamics, decongestion of a muscle will occur when intramuscular hydrostatic pressure exceeds intesdtitial osmotic pressure+venous/lymphatic hydrostatis pressure. A fluid outpouring into circulation reduces intramuscular congestion. Increasing intramuscular fluid pressure is achieved simply by reducing the volume of the muscle/container. The volume of a muscle/container is reduced when the walls are compressed inward. The greater the reduction in volume of a muscle/container, the more pressure the container's contents possess. The decongestive compression process works much like squeezing fluid from a mop where greater pressure applied yields a greater outpouring of fluid.
Incremental pressures applied using prior art are distributed over a small area, such that the pounds per square inch (PSI) are relatively elevated. But since soft muscle tissue can only tolerate so many PSI's before tissue damage and pain occur. Therefore, while large amounts of PSI pressure are generated by the small contact surface areas of prior art, only a fraction of the potential pressures are physically tolerable.
It is thus apparent that the need exists for na improved device for stimulating intramuscular fluid pressure or the like which provides relief from pain or other discomfort beyond that attainable through the use of prior art devices and methodology of use.